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Dengue Virus Infection Pathogenesis

This schematic diagram summarizes the pathophysiology of dengue fever and dengue hemorrhagic fever. It shows that dengue virus is transmitted via the bite of an infected Aedes aegypti mosquito. After entering the bloodstream, the virus replicates in immune cells and then targets the liver and spleen, causing apoptosis. This results in increased capillary permeability and plasma leakage. It also directly infects bone marrow cells, impairing platelet production. The combination of plasma leakage and thrombocytopenia can lead to life-threatening bleeding complications.
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0% found this document useful (0 votes)
400 views5 pages

Dengue Virus Infection Pathogenesis

This schematic diagram summarizes the pathophysiology of dengue fever and dengue hemorrhagic fever. It shows that dengue virus is transmitted via the bite of an infected Aedes aegypti mosquito. After entering the bloodstream, the virus replicates in immune cells and then targets the liver and spleen, causing apoptosis. This results in increased capillary permeability and plasma leakage. It also directly infects bone marrow cells, impairing platelet production. The combination of plasma leakage and thrombocytopenia can lead to life-threatening bleeding complications.
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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  • Pathogenesis of Dengue Virus: Flowchart illustrating the schematics of how dengue virus spreads, emphasizing environmental and vector factors.
  • Hematological Impact of Dengue: Diagram showing how dengue affects the hematological systems, focusing on fever, blood cell interactions, and thrombocytopenia.
  • Clinical Manifestations of Dengue: Continues with diagrams showcasing symptoms and clinical manifestations from dengue infection.
  • Inflammatory Response Mechanism: Flowchart diagram explaining the inflammatory response and associated symptoms in dengue fever.

Schematic Diagram

Predisposing Precipitating
Geographical area – tropical islands in the Environmental conditions (squatters area in Tondo,
Pacific (Philippines) and Asia Manila)
Vendor
Mosquito carrying dengue virus

Aedes aegypti (dengue virus carrier): 8-12 days of Bite from mosquito (Portal of Entry in the Skin)
viral replication on mosquitos’ salivary glands

Enters lymph circulation and into the blood.


(Viremia) The virus will bind to Antigen presenting cells (Langerhans cells), will
perform phagocytosis through Fc receptor (FcR) within the cells and
dengue virus replicates in the cells of macrophages. (Incubation
period: 3-14 days)
Recognition of dengue viral antigen on
infected cells by cytotoxic T cells Diagnostic:
Direct invasion of the virus and Hematology :
inflammatory process. Decreased
WBC:3,400
Release of cytokines which consist of
inflammatory agents such as interleukins, tumor
Decreased WBC
Dilation of Joint and muscle necrosis factor alpha, IFN gamma which
capillaries pain, headache, stimulates WBCs and pyrogen release (Imbalance
retro-orbital profile of cytokine and other mediators.)
pain,Nausea and Entry to the DENV infection of Bone marrow
vomiting spleen, and liver
Centrifugal
Pyrogens increase the production of
morbiliform
exanthema interleukin-1 (IL-1) in phagocytic cells.

Infection of stromal Direct infection of


cells progenitor cells
Pro inflammatory molecules IL-1 acts on the anterior hypothalamus
Virus ultimatelytotargets
increase
liver and spleen Impaired Decreased
(TNF-α, IL-6, IL-8 and IFN-γ) the production of prostaglandins
parenchymal cells where infection megakaryopoiesis megakaryopoiesis
Increase of set-
disrupt glycocalyx of produces apoptosis/cell death.
point temperature
endothelial cells
Decreased platelet production

Heat-generating Hepatosplenomegaly
mechanisms Signs/ symptoms:
allowing plasma to reach the
underlying intercellular junctions >Painful to palpate
abdomen in RUQ
and leak out of the blood vessel.
Fever
Blood Chemistry:
SGOT: 235.0 U/L(Up to
Plasma leakage
46)
including plasma Increased
SGPT:199 U/L(Up to 40)
proteins metabolic rate INR: 1.55
Increased PT,PTT Sequestration in
Moderate enlarged spleen
dehydration
Tachycardia
Decreased
intravascular
Development of anti-platelet
blood volume
antibodies of IgM isotype
Platelet
destruction
Drop in blood Thrombocytopenia
pressure from
initial 120/82 Direct invasion of platelets by DENV (DHF)
to 98/60 Decreased lung
Slight Dyspnea expansion due to
increase abdominal
Damage in blood vessels
pressure
Diagnostic:
Hematology :
Decreased Platelet:
Epistaxis 61,000/mmᵌ(150,00
Vomiting of blood (upper GI 0-400,000)
bleed) Increased PT,PTT
Hematochezia (lower GI bleed)
Subconjuctival hemorrhage
DENV infection of Bone marrow

Direct infection of
progenitor cells Infection of stromal cells

Decreased megakaryopoiesis Impaired megakaryopoiesis


Development of anti-platelet
antibodies of IgM isotype

Decreased platelet production

Platelet destruction

Thrombocytopenia

Direct invasion of platelets by DENV

Sequestration in enlarged spleen


Damage in blood vessels
Diagnostic:
Hematology :
Decreased Platelet:
Epistaxis 61,000/mmᵌ(150,00
Vomiting of blood (upper GI 0-400,000)
bleed) Increased PT,PTT
Hematochezia (lower GI bleed)
Subconjuctival hemorrhage

Schematic Diagram

Predisposing Precipitating
Geographical area – tropical islands in the Environmental conditions (squatters area in Tondo,
Pacific (Philippines) and Asia Manila)
Vendor
Mosquito carrying dengue virus
Aedes aegypti (dengue virus carrier): 8-12 days of Bite from mosquito (Portal of Entry in the Skin)
viral replication on mosquitos’ salivary glands

Enters lymph circulation and into the blood. The virus will bind to Antigen presenting cells (Langerhans cells), will
(Viremia)
perform phagocytosis through DC SIGN or Mannose type receptor
within the cells and dengue virus replicates in the cells of
macrophages. (Incubation period: 3-14 days)
Recognition of dengue viral antigen on
infected cells by cytotoxic T cells

Inflammatory Response to Dengue


Release of cytokines which consist of
inflammatory agents such as interleukins, tumor
Joint and necrosis factor alpha, IFN gamma which
muscle pain stimulates WBCs and pyrogen release (Imbalance
profile of cytokine and other mediators.)
Direct invasion of the virus and
inflammatory process. Pyrogens increase the production of
interleukin-1 (IL-1) in phagocytic cells.

Dilation of Dilation of intracranial IL-1 acts on the anterior hypothalamus to increase


capillaries blood vessels the production of prostaglandins

Increased ICP Increase of set-


Centrifugal point temperature
morbiliform
exanthema

Nausea and Heat-generating


vomiting mechanisms
headache,
retro-orbital
pain

Fever

Increased
metabolic rate

Moderate Tachycardia
dehydration

Slight Dyspnea

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